Mitochodrial anchor protein affects virulence of Candida albicans

Candida albicans is a major cause of fungal infections in humans and plays a significant role in fungal-related deaths due to its ability to form filaments and mask its cell wall, which are controlled by multiple signaling pathways. However, the relationship between mitochondria, filamentation, and cell wall masking in C. albicans is not fully understood. Therefore, we first determined that the mitochondrial anchor protein Num11 greatly affects filamentation and cell wall masking in C. albicans, both of which are crucial factors for infection. We then discovered that the loss of Num11 increases the ingestion of macrophages and decreases pathogenic activities in vivo. Interestingly, we found that the anchor protein Num1 can regulate the cAMP-PKA pathway to promote the growth of hyphal forms, influencing the Cdc42-Cek1 MAPK pathway to affect the production and presentation of polysaccharide components in the cell wall. Through these powerful mechanisms, the mitochondrial anchor protein Num11 significantly contributes to the pathogenicity of C. albicans. Our research also highlights the potential of Num1 as a new target for antifungal agents in the face of the ongoing challenge of drug-resistant fungi.